Severe propylene glycol toxicity secondary to use of anti-epileptics.

Propylene glycol toxicity presenting as high anion gap metabolic acidosis and osmolar gap has been extensively reported in literature, and most of them are secondary to intravenous lorazepam infusion. However, propylene glycol is used as a solvent in a number of medications that are frequently utilized in critical care setting, and hence one should be aware that the toxicity is possible from a variety of medication. Phenobarbital and phenytoin are one of those, and we hereby report a novel case of propylene glycol toxicity secondary to phenobarbital and phenytoin infusion in a patient with refractory status epilepticus. Furthermore, our patient had end-stage renal disease, which we think could have been an important precipitating factor for the toxicity. Because most of the symptoms from propylene glycol toxicity can mimic sepsis-which is very common in critical care unit patients-this life threatening scenario could be easily missed. Regular monitoring of osmolar gap is an easily available intervention in the at risk patients.

Epidemiology of bloodstream infections caused by Acinetobacter baumannii and impact of drug resistance to both carbapenems and ampicillin-sulbactam on clinical outcomes.

Acinetobacter baumannii has become a leading cause of bloodstream infections (BSI) in health care settings. Although the incidence of infection with carbapenem- and ampicillin-sulbactam-resistant (CASR) A. baumannii has increased, there is a scarcity of studies which investigate BSI caused by CASR A. baumannii. A retrospective cohort study was conducted on adult patients with BSI caused by A. baumannii and who were admitted to the Detroit Medical Center between January 2006 and April 2009. Medical records were queried for patients' demographics, antimicrobial exposures, comorbidities, hospital stay, and clinical outcomes. Bivariate analyses and logistic regression were employed in the study. Two hundred seventy-four patients with BSI caused by A. baumannii were included in the study: 68 (25%) caused by CASR A. baumannii and 206 (75%) caused by non-CASR A. baumannii. In multivariate analysis, factors associated with BSI caused by CASR A. baumannii included admission with a rapidly fatal condition (odds ratio [OR] = 2.83, 95% confidence interval [CI] = 1.27 to 6.32, P value = 0.01) and prior use of antimicrobials (OR = 2.83, 95% CI = 1.18 to 6.78, P value = 0.02). In-hospital mortality rates for BSI caused by CASR A. baumannii were significantly higher than those for non-CASR A. baumannii-induced BSI (43% versus 20%; OR = 3.0, 95% CI = 1.60 to 5.23, P value < 0.001). However, after adjusting for potential confounders, the association between BSI caused by CASR A. baumannii and increased risk of in-hospital mortality was not significant (OR = 1.15, 95% CI = 0.51 to 2.63, P value = 0.74). This study demonstrated that CASR A. baumannii had a distinct epidemiology compared to more susceptible A. baumannii strains; however, clinical outcomes were similar for the two groups. Admission with a rapidly fatal condition was an independent predictor for both CASR A. baumannii and in-hospital mortality.

Outbreak of colistin-resistant, carbapenem-resistant Klebsiella pneumoniae in metropolitan Detroit, Michigan.

Carbapenem-resistant Klebsiella pneumoniae has spread worldwide and throughout the United States. Colistin is used extensively to treat infections with this organism. We describe a cluster of colistin-resistant, carbapenem-resistant K. pneumoniae infection cases involving three institutions in Detroit, MI. A cluster of five cases of colistin-resistant, carbapenem-resistant K. pneumoniae was identified at Detroit Medical Center (DMC) from 27 July to 22 August 2009. Epidemiologic data were collected, and transmission opportunities were analyzed. Isolates were genotyped by using pulsed-field gel electrophoresis and repetitive extragenic palindromic PCR. Data regarding the use of colistin were obtained from pharmacy records. The index case of colistin-resistant, carbapenem-resistant K. pneumoniae was followed 20 days later by four additional cases occurring in a 6-day interval. All of the patients, at some point, had stayed at one particular institution. The mean number of opportunities for transmission between patients was 2.3 ± 0.5, and each patient had at least one opportunity for transmission with one of the other patients. Compared to 60 colistin-susceptible, carbapenem-resistant K. pneumoniae controls isolated in the previous year at DMC, case patients were significantly older (P = 0.05) and the carbapenem-resistant K. pneumoniae organisms isolated from them displayed much higher MICs to imipenem (P < 0.001). Colistin use was not enhanced in the months preceding the outbreak. Genotyping revealed two closely related clones. This report of a colistin-resistant, carbapenem-resistant K. pneumoniae outbreak is strongly linked to patient-to-patient transmission. Controlling the spread and novel emergence of bacteria with this phenotype is of paramount importance.